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作 者:曹影[1] 王培蓓[1] 马荧雪[1] 谭长强 陈智斌[1]
机构地区:[1]南京医科大学第一临床医学院耳鼻咽喉头颈外科,江苏省210029 [2]南京鼓楼医院耳鼻咽喉头颈外科
出 处:《江苏医药》2013年第9期1015-1017,共3页Jiangsu Medical Journal
摘 要:目的研究miR-137对喉癌细胞株Hep-2细胞增殖及细胞周期的影响。方法将Hep-2细胞分为转染miR-137寡聚核苷酸组(A组)、转染无义序列组(B组)和空白对照组(C组)。采用RT-PCR、MTT法、流式细胞仪和Western blot技术评价各组细胞增殖和细胞周期的生物学特征。结果转染miR-137寡聚核苷酸后,Hep-2细胞中miR-137表达显著增加。与C组相比,A组细胞增殖水平明显抑制,miR-137寡聚核苷酸能够有效诱导Hep-2细胞周期阻滞在G1/G0期;A组细胞分裂周期蛋白42表达水平明显下调,细胞周期调控因子蛋白CDK4及细胞周期素D1蛋白表达水平明显降低。结论 miR-137寡聚核苷酸能够显著抑制喉癌细胞Hep-2的增殖,miR-137是潜在的人喉癌细胞基因治疗的候选靶点。Objective To investigate the impact of miR-137 on proliferation of laryngeal carcinoma cell line Hep-2 cells. Methods The oligonueleotide of miR-137 was transfected into laryngeal carcinoma cell line Hep-2 cells, which were derided into three groups of A(miR-137 transfection),B(non-serial transfection) and C(blank control). The expression of miR-137 was defected by RT-PCR, and relevant protein expression was evaluated by Western blot. The cell proliferation and cell cycle were determined by MTT assay and flow cytometry, respectively. Results Compared to group C, miR-137 expression in Hep-2 cells was obviously elevated atter miR-137- transfeeted. The proliferation of Hep-2 cells in group A was significantly inhibited and the cell cycle arrested at G0/G1 phase. The protein expression of CDC42 was downregulated with decreased expressions of CDK4 and cyelin D1 in group A . Conclusion MiR-137 inhibits the proliferation activity of Hep-2 cells, suggesting that miR-137 can be taken as a potential candidate for gene therapy of laryngeal carcinoma.
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